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10.3109/17435390.2014.976603 http://scihub22266oqcxt.onion/10.3109/17435390.2014.976603 C4800815!4800815 !25387250     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25387250 &cmd=llinks): Failed to open stream: HTTP request failed! 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Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary co-culture model |pdf=|usr=}}{{25387250 }} gab.com Text Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary co-culture model JO: Nanotoxicology http://www.kidney.de/pget.php?&tw=1&pmid=25387250 #FOAvip The printer is one of the most common office equipment. Recently, it was reported that toner formulations for printing equipment constitute nano-enabled products (NEPs) and contain engineered nanomaterials (ENMs) that become airborne during printing. To date, insufficient research has been performed to understand the potential toxicological properties of printer-emitted particles (PEPs) with several studies using bulk toner particles as test particles. These studies demonstrated the ability of toner particles to cause chronic inflammation and fibrosis in animal models. However, the toxicological implications of inhalation exposures to ENMs emitted from laser printing equipment remain largely unknown. The present study investigates the toxicological effects of PEPs using an in vitro alveolar-capillary co-culture model with Human Small Airway Epithelial Cells (SAEC) and Human Microvascular Endothelial Cells (HMVEC). Our data demonstrate that direct exposure of SAEC to low concentrations of PEPs (0.5 and 1.0?µg/mL) caused morphological changes of actin remodeling and gap formations within the endothelial monolayer. Furthermore, increased production of reactive oxygen species (ROS) and angiogenesis were observed in the HMVEC. Analysis of cytokine and chemokine levels demonstrates that interleukin (IL)-6 and MCP-1 may play a major role in the cellular communication observed between SAEC and HMVEC and the resultant responses in HMVEC. These data indicate that PEPs at low, non-cytotoxic exposure levels are bioactive and affect cellular responses in an alveolar-capillary co-culture model, which raises concerns for potential adverse health effects. Twit Text FOAVip Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary co-culture model ????Nanotoxicology http://www.kidney.de/pget.php?&tw=1&pmid=25387250 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25387250 #FOAvip English Wikipedia <ref>{{Cite pmid|25387250 }}</ref> Small airway epithelial cells exposure to printer-emitted engineered nanoparticles induces cellular effects on human microvascular endothelial cells in an alveolar-capillary co-culture model #MMPMID25387250 Sisler JD ; Pirela SV ; Friend S ; Farcas M ; Schwegler-Berry D ; Shvedova A ; Castranova V ; Demokritou P ; Qian Y Nanotoxicology 2015[]; 9 (6 ): 769-79 PMID25387250 show ga The printer is one of the most common office equipment. Recently, it was reported that toner formulations for printing equipment constitute nano-enabled products (NEPs) and contain engineered nanomaterials (ENMs) that become airborne during printing. To date, insufficient research has been performed to understand the potential toxicological properties of printer-emitted particles (PEPs) with several studies using bulk toner particles as test particles. These studies demonstrated the ability of toner particles to cause chronic inflammation and fibrosis in animal models. However, the toxicological implications of inhalation exposures to ENMs emitted from laser printing equipment remain largely unknown. The present study investigates the toxicological effects of PEPs using an in vitro alveolar-capillary co-culture model with Human Small Airway Epithelial Cells (SAEC) and Human Microvascular Endothelial Cells (HMVEC). Our data demonstrate that direct exposure of SAEC to low concentrations of PEPs (0.5 and 1.0?µg/mL) caused morphological changes of actin remodeling and gap formations within the endothelial monolayer. Furthermore, increased production of reactive oxygen species (ROS) and angiogenesis were observed in the HMVEC. Analysis of cytokine and chemokine levels demonstrates that interleukin (IL)-6 and MCP-1 may play a major role in the cellular communication observed between SAEC and HMVEC and the resultant responses in HMVEC. These data indicate that PEPs at low, non-cytotoxic exposure levels are bioactive and affect cellular responses in an alveolar-capillary co-culture model, which raises concerns for potential adverse health effects. |*Printing [MESH] |Air Pollutants/chemistry/*toxicity [MESH] |Capillaries/cytology/drug effects/immunology [MESH] |Cell Line [MESH] |Cell Survival/drug effects [MESH] |Coculture Techniques [MESH] |Cytokines/metabolism [MESH] |Dose-Response Relationship, Drug [MESH] |Endothelial Cells/*drug effects/immunology/pathology [MESH] |Endothelium, Vascular/drug effects/immunology/pathology [MESH] |Epithelial Cells/drug effects/immunology/pathology [MESH] |Humans [MESH] |Microscopy, Confocal [MESH] |Microvessels/*drug effects/immunology/pathology [MESH] |Nanoparticles/chemistry/*toxicity [MESH] |Particle Size [MESH] |Pulmonary Alveoli/drug effects/immunology/pathology [MESH] |Respiratory Mucosa/blood supply/*drug effects/immunology/pathology [MESH]Small airway epithelial cells exposure to printer-emitted engineered (epmc).pdf DeepDyve Pubget Overpricing